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1.
The nature, occurrence and effects of nephrotoxic mycotoxins are considered at their different levels of involvement in animal renal disease. The four associated with field outbreaks of nephrotoxicosis, viz. ochratoxin A, citrinin, aflatoxin and oxalic acid are mainly produced by Aspergilli and Penicillia in grain and other crops, e.g. peanuts. Ten nephrotoxins detected by experimentation including cyclopiazonic acid, penicillic acid and viridicatumtoxin, may also eventually be found to play a role in these diseases. Thirteen fungi frequently isolated from foodstuffs have produced renal (mostly tubular) lesions on the feeding of cultures to animals, in the absence of known nephrotoxins. The pathological changes reported have been predominantly in the proximal tubules with profound cytoplasmic and nuclear effects. The relationship of porcine nephropathy (due to ochratoxin A) to Balkan Nephropathy and the associated urinary tract tumours in man is discussed and the close parallel to the carcinogenic hepatoxicity of the aflatoxins indicated.  相似文献   

2.
Twenty-one pigs weighing approximately 18 kg were placed in 7 groups of 3 and given diets containing respectively aflatoxin B1 alone at 0.375 and 0.0750 mg/kg, ochratoxin A alone at 1 and 2 mg/kg, 0.375 mg/kg of aflatoxin B1 plus 1 mg/kg of ochratoxin A and 0.750 mg/kg aflatoxin B1 and 2 mg/kg of ochratoxin A. The remaining group served as untreated control. At the respective dose levels, pigs receiving similar doses of ochratoxin A alone or in combination with aflatoxin B1, were similarly affected, the clinical effects of aflatoxin having been mostly obscured by those due to ochratoxin A. Mild degenerative hepatic changes typical of aflatoxicosis were observed in pigs fed this toxin alone or in combination with ochratoxin A. In kidneys of pigs fed diet containing 1 and 2 mg of ochratoxin A alone changes included interstitial fibrosis of the vortex and dystrophy and degeneration of the tubular epithelium. Similar lesions but less pronounced fibrosis were found in kidneys of pigs receiving both toxins. The respective lower dose levels of mycotoxins selected were judged to be about the no-effect levels for each dosed separately under the conditions of the trial. Such levels have been found not infrequently on mould affected grain and stock foods. The result highlights the difficulties that may be experienced in the recognition of such multimycotoxicoses as they are likely to occur in the field and indicate the need for toxicological analysis as well as pathological investigation in establishing a diagnosis.  相似文献   

3.
Fourteen pigs were fed ochratoxin A and citrinin through a stomach tube at daily doses of 0.02 and 0.01 mg/kg body mass for 57 days. These toxin doses correspond to the average toxin contamination level of feeds in Central Europe. The clinical status of the pigs was monitored and clinical laboratory, haematological and mycotoxin-analytical examinations were performed throughout the trial. At the end of the experiment gross and histopathological examinations were carried out. The results of ochratoxin A and citrinin determination in the blood, obtained by high-performance liquid chromatography (HPLC), are important from the food hygienic point of view. The sensitivity of the method was 2 and 10 ng/ml for ochratoxin A and citrinin, respectively. The recovery rate of the mycotoxins was above 60%.  相似文献   

4.
Two gopher snakes (Pitophis melanoleucus catenifer) each were given 5 mg/kg body weight gentamicin every 72 hours (group 1); two snakes each were given 5 mg/kg/day (group 2). Doses for both groups were given over a 2-week period. After the second week, the dose for one snake in each group was increased to 50 mg/kg/day for 2 more weeks and then discontinued. Weekly renal biopsies taken from snakes in group 1 showed no abnormalities by light microscopy during and at the completion of the experiment. Snakes in group 2 had cloudy swelling of the proximal tubules at 2 and 4 weeks after the gentamicin was administered. Snakes given the high dose of gentamicin had hydropic degeneration of the proximal tubules 2 weeks after the dose was raised to 50 mg/kg/day. This progressed to tubular necrosis 1 week after the gentamicin was discontinued. These snakes (high dose) also developed visceral gout, apparently as the result of the extensive tubular necrosis. Tophi were in the pericardium, serosal membranes and parenchyma of the kidneys, liver, spleen and lungs.  相似文献   

5.
The lesions caused by excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day), given individually and in combination to adult Beagle dogs, were evaluated. The experimental period was 100 to 112 days, except that four dogs in each of the clioquinol and combined-treatment groups were killed early because of severe debilitation or neurologic disease, and one dog given both compounds died on the third day of compound administration. Degenerative neurologic lesions had distribution specific for the compound given. Pyridoxine-treated dogs had lesions limited to tracts and nerves with neuronal bodies of their nerve fibers in the spinal and trigeminal ganglia. Clioquinol-treated dogs had neurologic lesions limited to the central nervous system. The most lesions were in the rostral dorsal funiculus and distal aspects of the optic nerve fibers, but minimal to mild degenerative changes also occurred in distal aspects of the corticospinal and spinocerebellar tracts. Dogs given both pyridoxine hydrochloride and clioquinol had a combination of the lesions in dogs given pyridoxine or clioquinol individually. Several dogs given clioquinol or pyridoxine plus clioquinol had extraneural lesions, including myocardial degeneration and thyroidal alterations.  相似文献   

6.
1. Toxic effects of two concentrations (0.5 and 1 mg/kg) of ochratoxin A (OTA) and attenuating effects of a toxin deactivator (Mycofix Plus(MTV INSIDE)) containing the yeast Trichosporon mycotoxinivorans on the performance (feed conversion ratio; body weight gain), serum enzymes (lactate dehydrogenase, gamma-glutamyltranspeptidase and aspartate aminotransferase) and clinico-pathomorphology of internal organs were studied in 270 one-day-old broiler chicks divided into 9 groups over a 42-d period. 2. Feed conversion ratios (FCR) in groups fed toxin deactivator were improved compared with groups receiving OTA only. An increase in the relative weight of kidney and liver was observed in groups fed 0.5 and 1 mg/kg OTA on day 42 of the experiment as compared with the control group. In contrast, relative weights of bursa of Fabricius and spleen were not significantly affected in experimental groups exposed to OTA as compared to control groups determined on days 28 and 42 of age. 3. Serum enzymes (LDH, GGT and AST) values in OTA treated groups determined on days 28 and 42 were higher than those of the control group. 4. Histopathological examination of kidney on day 42 revealed degenerative changes in the epithelial cells of the proximal convoluted tubules and massive necrosis of the proximal tubular epithelial cells. These changes were less marked in birds receiving 0.5 mg/kg OTA than in those receiving 1 mg/kg. In general, histological changes in kidneys, liver, bursa and spleen were less pronounced in birds receiving OTA and toxin deactivator concomitantly. 5. Dietary OTA at 0.5 and 1 mg/kg adversely affects FCR, increases the serum liver enzymes and induces pronounced pathomorphological and histological changes in internal organs of broiler chicks. Co-administration of OTA with deactivator attenuated the harmful effects.  相似文献   

7.
Citrinin mycotoxicosis in the rabbit: ultrastructural alterations   总被引：1，自引：0，他引：1  
Citrinin was given to rabbits as a single oral dose of 120 or 67 mg/kg. Rabbits were killed at 4, 6, 8, 10, and 12 hours post dosing, and the kidneys were fixed by intravascular perfusion. Ultrastructural alterations were evident by 4 hours after treatment. In the proximal tubule, alterations were brush border disruption, cytoplasmic rarefaction, and swelling of interdigitating processes. At higher doses, mitochondria were condensed and distorted. Medullary and straight cortical distal tubules had marked distention of the intercellular spaces and disorganization of interdigitating processes. Changes in cortical and outer medullary collecting ducts were similar but less severe. Renal alterations were suggestive of damage to membrane structure and/or transport functions and interference with cellular bioenergetics. Leukocytic infiltration was associated with damaged tubules indicating a contribution of inflammation to the development of the lesions.  相似文献   

8.
Nine pigs were fed crystalline ochratoxin A in their feed at a concentration of about 1 mg/kg. Three pigs and their controls were killed after 3 months and 6 pigs and controls were killed after 2 years. A decrease of the ratio TmPAH/CIn, increased urinary glucose excretion and decreased ability to concentrate urine, occurred within a few weeks and aggravated slightly during the 2-year period. Changes in renal structure, characterized by degeneration and atrophy of proximal tubules, interstitial fibrosis and hyalinization of glomeruli, were progressive during time of exposure, but terminal renal failure was not reached. The kidney, liver, muscular and adipose tissue contained 3 to 27 microgram ochratoxin A/kg after 3 months of exposure. No further accumulation of ochratoxin A residue was found after 2 years of exposure.  相似文献   

9.
Hemorrhagic fever with renal syndrome (HFRS) virus, strain SR-11 (SR) was inoculated intraperitoneally into specific-pathogen-free (SPF) newborn rats, from which the kidney lesions were examined pathologically. The infected rats revealed proteinuria on and after 16 days postinoculation (PI). Histologically, the epithelial cells of the renal tubules showed mild vacuolar and granular degeneration with cytoplasmic inclusion bodies (CIB) on and after 16 days PI. Ultrastructurally, a decrease in number of mitochondria and endocytic vesicles was recognized in the epithelial cells of the proximal renal tubules. Occasionally, both the proximal and distal renal tubular cells had CIB near well-developed Golgi apparatus on and after 13 days PI. Immunohistochemically, CIB were positive for anti-SR nucleocapsid antibody, but negative for anti-SR envelope protein antibody. From the results obtained here, it was concluded that the proteinuria in rats infected with HFRS virus resulted from an insufficiency of reabsorption in the proximal renal tubules, and that CIB consisted of the viral nucleocapsid protein.  相似文献   

10.
Sixteen animals affected in 2 outbreaks of pet food-associated renal failure (2 dogs in 2004; 10 cats and 4 dogs in 2007) were evaluated for histopathologic, toxicologic, and clinicopathologic changes. All 16 animals had clinical and laboratory evidence of uremia, including anorexia, vomiting, lethargy, polyuria, azotemia, and hyperphosphatemia. Where measured, serum hepatic enzyme concentrations were normal in animals from both outbreaks. All animals died or were euthanized because of severe uremia. Distal tubular lesions were present in all 16 animals, and unique polarizable crystals with striations were present in distal tubules or collecting ducts in all animals. The proximal tubules were largely unaffected. Crystals and histologic appearance were identical in both outbreaks. A chronic pattern of histologic change, characterized by interstitial fibrosis and inflammation, was observed in some affected animals. Melamine and cyanuric acid were present in renal tissue from both outbreaks. These results indicate that the pet food-associated renal failure outbreaks in 2004 and 2007 share identical clinical, histologic, and toxicologic findings, providing compelling evidence that they share the same causation.  相似文献   

11.
The toxic effects of imidocarb diproprionate (3,3'-bis [2 imidazolin-2yl]-carbanilde diproprionate) were evaluated in adult goats given (intramuscular injection) a lethal dose (6.75 mg/kg). The immediate clinical signs of toxicosis were transient excessive salivation and diarrhea. Anorexia, dyspnea, recumbency, and death occurred between postinjection days (PID) 4 and 8, during which time 7 goats died and 4 moribund goats were euthanatized. There were marked increases in mean serum urea nitrogen concentration and significant increases in serum glutamic oxalacetic transminase activity and in the mean number of circulating neutrophils after PID 4. Renal hyperemia and enlargement were evident by PID1. Serosanguineous fluid in the trachea and major bronchi, pulmonary congestion and edema, hydrothorax, hydroperitoneum, and less frequently hydropericardium were observed on and after day 4. Microscopic renal tubular lesions rapidly progressed from pyknotic epithelial nuclei observed at 6 and 12 hours to acute tubular necrosis of epithelium of the proximal convoluted tubules on days 1 and 2. Pulmonary congestion and edema; hemorrhage into alveoli, bronchioles, and bronchi; and intracytoplasmic lipid vacuoles within the hepatocytes in the periacinar zones of the hepatic lobules were observed on or after day 4. Succinic dehydrogenase and adenosine triphosphatase activities decreased progressively in the epithelial cells of the proximal convoluted tubules. The decreases in cellular enzymatic activity occurred shortly after the appearance of microscopic lesions in the tubular epithelium.  相似文献   

12.
Kidneys from broiler chicks receiving 300 micrograms of oosporein K salt per gram of feed continuously from 0 to 21 days of age were examined by light and electron microscopy. Chicks that died at 3 days had nephrosis of initial proximal tubular segments with an early pyogranulomatous interstitial response. Macula densa cells had cytoplasmic accumulations of periodic-acid-Schiff-positive granules. Kidneys from chicks surviving 21 days had hypercellular or atrophic glomeruli and hyperplastic dilated proximal tubules. Centrilobular distal tubules were dilated and filled with hyaline basophilic casts. Interstitial fibrosis was prominent in cortical and medullary zones. These findings indicate that oral oosporein is a severe nephrotoxin which can cause visceral urate deposition and severe nephrosis of initial proximal tubular segments. The histopathology of this mycotoxicosis was compared with those of infectious-bronchitis-induced nephrosis and avian urolithiasis syndrome.  相似文献   

13.
Total water deprivation of 2-day-old broiler chicks for 24, 48, 72, 96, and 120 hours did not result in visceral urate deposits. Renal tubular changes consisted of increased spaces between membrane infoldings of the distal convoluted tubular epithelium, increased number of cytoplasmic vacuoles in proximal convoluted tubules, and increased mucin production and dilation of collecting ducts.  相似文献   

14.
Lithium chloride was given intraperitoneally to dogs at a dosage of 125 mg/kg body weight for three days. Kidneys were removed for morphologic examination and quantitation of sodium-potassium-adenosine triphosphatase (Na-K-ATPase) activities in cortical and medullary tissue. Light microscopy showed no changes in the kidneys, but cytoplasmic vacuolation and dilatation of the cisternae of the endoplasmic reticulum were seen ultrastructurally in the epithelial cells of the distal tubule and cortical and medullary collecting ducts. Mean cortical Na-K-ATPase activity was 1.49 +/- 0.25 and 1.70 +/- 0.31 mumoles inorganic phosphate/mg protein/hour in control and experimental groups respectively. Mean medullary Na-K-ATPase activity was 4.71 +/- 0.41 and 5.01 +/- 0.47 mumoles inorganic phosphate/mg protein/hour in control and experimental groups respectively. It was concluded that lithium produced morphologic changes in the distal nephron, but had no effect on renal Na-K-ATPase activity.  相似文献   

15.
A sublethal dose of ethylene glycol was administered orally to 3 groups of dogs; dogs of a control group were given distilled water instead. Renal cortical biopsy samples were obtained from dogs of experimental and control groups at various times after treatment. Tissue was examined by use of light microscopy and transmission electron microscopy. In dogs of the control group, the light and electron microscopic appearances of tissue were within normal limits at all sample collection hours. In dogs of the experimental groups, renal corpuscular structure remained within normal limits by use of light and electron microscopy throughout the study, though morphologic change was seen in other structures of the cortex. Light microscopic lesions first appeared at 12 hours, and were similar to those reported in the literature. Ultrastructural lesions were first observed in the 5-hour samples, and similar to the light microscopic lesions, were most common in the proximal convoluted tubules (PCT). Initial PCT cellular changes included vacuolization of cells and distention of the parabasal extracellular spaces; PCT cellular lesions seen in later-hour samples included formation of apical buds and cellular rupture. Internalization or sloughing of the PCT brush border was not observed. Distal convoluted tubules (DCT) were frequently dilated and/or packed with cellular debris. A few DCT cells had degenerative or necrotic changes. In PCT and DCT, abnormal cells were frequently flanked by normal or nearly normal cells. During later hours, a few cells with types of changes first observed in early hours continued to be observed, implying ongoing response of cells to the toxin.  相似文献   

16.
Ultrastructural changes are reported in the kidney and liver of 20-day-old broiler chicks fed ochratoxin A (OA), incorporated in the diet at levels of 2 and 4 ppm. Changes in the kidney included the presence of abnormally shaped mitochondria in the proximal convoluted tubules. There was an increase in the size and number of mitochondrial dense granules and cytoplasmic peroxisomes. Intranuclear and cytoplasmic lipid droplets and electron dense round bodies in the dilated smooth endoplasmic reticulum were also noted. Regional thickening and degeneration of the glomerular basement membrane was observed in some cases. In the liver from OA fed birds there was an increased accumulation of cytoplasmic glycogen in the hepatocytes. Abnormal mitochondrial ring forms in the kidney and the accumulation of glycogen in the liver are considered to be of diagnostic significance in ochratoxicosis of young broiler chicks. The severity of the changes was found to be dose related. These results suggest that the mitochondria in the proximal convoluted tubules of kidney were most sensitive to OA toxicity.  相似文献   

17.
Twelve Nubian goats were given single or repeated oral dosages of mercuric chloride at 10, 20 and 40 mg/kg and died or were killed in extremis at various times after dosing (18 hours-18 days). The main signs of poisoning were anorexia, frothing at the mouth, respiratory distress, epistaxis, bloat, diarrhoea, abnormal posture and recumbency. An increase in the activity of GOT and in the concentrations of urea and inorganic phosphate and a decrease in total protein and calcium concentrations in the serum were detected. The main lesions were dilatation and necrosis of the proximal convoluted tubules, shrinkage and disappearance of the glomerular tufts, varying amounts of acidophilic homogenous material in the lumens of the affected tubules of the kidney, enteritis, hepatocellular degeneration and/or necrosis and pulmonary congestion, haemorrhage, oedema and emphysema. The changes in the red blood cells indicated anaemia.  相似文献   

18.
Histological and electron microscopic examinations of the kidneys of 8 dogs suffering from fatal, naturally acquired Babesia canis infection and nephropathy are presented. Seven animals were treated with imidocarb dipropionate on average 4.5 days prior to death. Severe anaemia was present only in 2 cases. Degenerative histological changes observed mostly in the proximal convoluted tubules included vacuolar-hydropic degeneration, necrosis and detachment of renal tubular epithelial (RTE) cells from the basement membrane. Necrotic debris occasionally formed acidophilic casts within the tubules. In some cases, necrosis of the whole tubule was observed. Haemoglobin casts in the tubules and haemoglobin droplets in RTE cells seldom appeared. No significant histological changes were seen in the glomeruli. Ultrastructural lesions in RTE cells included nuclear membrane hyperchromatosis, karyopyknosis, karyolysis, swelling or collapse of mitochondria with fragmentation of cristae and vacuolar-hydropic degeneration in the endoplasmic reticulum and microvilli. Nuclear oedema was also observed. Many RTE cells exhibiting necrosis collapsed. Vacuolar-hydropic degeneration and necrosis were also observed in the glomerular and interstitial capillary endothelium. The severe acute tubular necrosis described in this study is probably the result of hypoxic renal injury. Systemic hypotension leading to vasoconstriction in the kidneys might be the most important cause of renal hypoxia in B. canis infections, but anaemia may also contribute to inadequate oxygenation. Imidocarb should be applied with caution in patients with possible renal involvement until further data become available on its potential nephrotoxicity in dogs.  相似文献   

19.
Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep poisoned by superphosphate containing approximately 1.5% fluoride. The LD50 of NaF was in the range 100 to 300 mg/kg (45 to 135 mg F/kg). This range is of the same order as the amount of fluoride in a toxic dose of superphosphate (70 to 90mg F/kg).

A lethal dose of NaF caused severe depression, salivation, hyperpnoea, blindness, ataxia and incoordination. Death ensued three to 52 hours after dosing. Acute necrotizing rumino-reticulitis and abomasitis and necrosis of epithelial cells in the proximal convoluted tubules of the kidney were the characteristic lesions of NaF toxicity.

Superphosphate poisoning took a more protracted course with depression and diarrhoea as the predominant clinical signs until the terminal coma. As with NaF, the notable lesions were in the gastrointestinal tract and kidneys, but were less severe.

Although there were differences in the clinical and pathological manifestations of the two forms of poisoning, the comparable toxic dose of NaF and of the fluoride in a toxic dose of superphosphate, and the similar target organs involved, support the view that fluoride plays a dominant role in the pathogenesis of superphosphate poisoning. It is probable that phosphate plays a contributory role but the nature of the interaction of fluoride and phosphate remains to be established.  相似文献   

20.
Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep poisoned by superphosphate containing approximately 1.5% fluoride. The LD50 of NaF was in the range 100 to 300 mg/kg (45 to 135 mg F/kg). This range is of the same order as the amount of fluoride in a toxic dose of superphosphate (70 to 90 mg F/kg). A lethal dose of NaF caused severe depression, salivation, hyperpnoea, blindness, ataxia and incoordination. Death ensued three to 52 hours after dosing. Acute necrotizing rumino-reticulitis and abomasitis and necrosis of epithelial cells in the proximal convoluted tubules of the kidney were the characteristic lesions of NaF toxicity. Superphosphate poisoning took a more protracted course with depression and diarrhoea as the predominant clinical signs until the terminal coma. As with NaF, the notable lesions were in the gastrointestinal tract and kidneys, but were less severe. Although there were differences in the clinical and pathological manifestations of the two forms of poisoning, the comparable toxic dose of NaF and of the fluoride in a toxic dose of superphosphate, and the similar target organs involved, support the view that fluoride plays a dominant role in the pathogenesis of superphosphate poisoning. It is probable that phosphate plays a contributory role but the nature of the interaction of fluoride and phosphate remains to be established.  相似文献   

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